Neurocardiogenic syncope (vasovagal syncope, the common “fainting spell”) is a common but complex physiologic disorder. An estimated 6% of the population are recurrent fainters. The condition is marked by a sudden drop in heart rate and blood pressure, resulting in decreased cerebral perfusion and subsequent loss of consciousness and postural tone. This condition is unpleasant and limiting for the patient as well as potentially dangerous; unexpected episodes of syncope may result in injury from falls. In addition, when frequent, it can lead to disability due to prohibitions on driving as well as certain types of employment and activities. Behavioral treatment for recurrent neurocardiogenic syncope has been limited to lifestyle limitation, avoidance behaviors and abortive maneuvers, and liberalization of fluid and sodium intake. Medical therapy has been limited to selective serotonin reuptake inhibitors and the “off label” use of fludrocortisone, a mineralocorticoid that enhances sodium and water retention. The latter therapy is often unacceptable in older patients with preexisting heart disease or hypertension.
Given the limitations of medical and behavioral therapy, some consideration has been given to the role of cardiac pacemakers in treating neurocardiogenic syncope. Since an abrupt drop in heart rate is a prominent feature of most neurocardiogenic syncopal episodes, prior devices and algorithms have focused on various “rate drop response” algorithms, in which the pacemaker detects when the patient's heart rate drops below a lower hysteresis rate and determines whether the rate of decrease in heart rate (dHR/dT) exceeds a predetermined value; if this condition is met, then the pacemaker output is set to the hysteresis rate for a preset time interval. However, as a whole, these therapies have yielded disappointing results.
Given that therapies have yielded inconsistent results, are largely disappointing and pacemakers remain unattractive therapy, the emphasis for this invention is on early recognition of impending syncope and diagnosis of syncopal episodes due to hypotension. Although monitoring of heart rate and rhythm is accomplished simply with a set of three leads applied to the chest (as is used on telemetry units and outpatient monitoring), there is as of yet no practical way of monitoring of intracranial blood flow, the final common pathway that is interrupted when syncope occurs. Additionally, monitoring of systemic blood pressure on a continuous basis, a less than ideal surrogate for intracranial blood flow, is also impractical or difficult in ambulatory individuals. The desire to monitor intracranial blood flow extends beyond diagnosis of patients with recurrent syncope; it also applies to monitoring of such individuals as fighter pilots, test pilots, in aerospace applications, hyperbaric situations and soldiers or first responders in the field.
Some known techniques involve head up tilt table testing to approximate the hemodynamic changes seen during neurocardiogenic syncope. Previous investigations have noted that, in addition to decreases in heart rate and blood pressure, changes in breathing patterns may also occur before fainting. Subjects have been observed to yawn, sigh, or hyperventilate before syncope, suggesting that alterations in respiration may accompany sudden changes in autonomic control of the heart and peripheral vasculature.
The causal relationship between respiratory variation and neurocardiogenic syncope has been unclear. Vasomotor instability preceding syncope has been previously discussed; however, early work did not show a convincing relationship between respiration and syncope in healthy volunteers. Studies using indirect measurement of minute ventilation and complex demodulation have demonstrated that hyperpnea precedes increases in cardiac vagal tone and subsequent decrease in intracranial blood flow and tilt-induced syncope in healthy volunteers. Prior work has shown excellent correlation between exhaled carbon dioxide levels and cerebral blood flow. Previous work also suggests a very reproducible pattern of changes in tidal volume without accompanying changes in respiratory rate, which very reliably predict impending syncope (real-time), diagnose a syncopal event as having occurred (after the fact) and act as an excellent surrogate of decreased cerebral perfusion.
The present invention contemplates elimination of drawbacks associated with prior methods and provision of a method of detecting neurocardiogenic syncope early enough so that avoidance maneuvers can be undertaken or, as of yet not described therapies can be instituted.